Sleep & focus · Nasal spray
N-Acetyl Selank
Gray market0 published studies
Clinical Use (Russia) for Selank, the parent · No data for this form · marketing claims
Gray market · No FDA ruling — not on any list
Sold as a research chemical.
Bottom line
Parent has the Russian clinical record. The capped version has no peer-reviewed validation of its own.
- Also called
- N-Acetyl Selank Amidate
- N-Ac-Selank-NH₂
- stabilized Selank analog
- Ac-TKPRPGP-NH₂
- Category
- Peptide — Tuftsin-Family Anxiolytic
- Parent Sequence
- Thr-Lys-Pro-Arg-Pro-Gly-Pro
- Modifications
- N-acetyl + C-amide
- Class
- Tuftsin analog glyproline
- Route (studied)
- No study of it
- Route (sold)
- Powder vials for nasal spray (research chemical)
- Half-life
- Not measured (no study of the capped analog)
- Parent FDA Status
- Not approved
- Parent Russia Status
- Approved (GAD, asthenia)
- Analog Clinical Trials
- None, and no published preclinical study either (PubMed, searched October 11, 2026)
- WADA Status
- Not specifically named — prohibited at all times under S0 (no government has approved it for human use)
- Cost & Access
- Research-only
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What does it do? The parent, Selank, is sold in Russia for anxiety states and asthenia (Russian product instructions). In rats and cells it shifts GABA-system gene activity (Volkova et al., 2016), changes BDNF in the hippocampus (Inozemtseva et al., 2008) and blocks the serum enzymes that break down enkephalins (Kost et al., 2001). What the caps change has not been measured in any published study.
Who uses it? In Russia the parent is sold without a prescription for anxiety states, asthenia and stress disorders (Russian product instructions). Biohacker and nootropic communities use the capped version via research-peptide vendors.
Does the evidence hold up? Parent Selank: a 2008 Russian randomized trial of 62 patients matched the benzodiazepine medazepam for anxiety, with added anti-fatigue effects (Zozulia et al., 2008). The capped version has no clinical trial of its own.
Bottom line? Parent has the Russian clinical record. The capped version has no peer-reviewed validation of its own.
Dosing from the Literature
Published for anxiety: parent Selank's Russian nasal dose, about 300 mcg a spray. Not published: any dose of the capped version.
The Russian instructions for the parent, Selank, give 2 drops of the 0.15% solution in each nostril three times a day, for 14 days (Russian product instructions). No dose of the capped version has been published.
| Application | Dose | Frequency | Notes |
|---|---|---|---|
| Parent Selank, Russian label (anxiety states, asthenia, stress disorders) | 0.15% nasal drops (1.5 mg/mL); 2 drops in each nostril | 3× daily | Russian product instructions: adults 18 and over; a 14-day course, repeatable after 1–3 weeks, after consulting a doctor. |
N-Acetyl Selank has no regulated dosing. The dose above is the parent’s, from its Russian label; no dose has been published for the capped analog. They are not clinical recommendations. Consult a licensed healthcare provider.
→ Calculator — vial-to-syringe math
What It Is
N-Acetyl Selank is a chemically modified analog of Selank — a synthetic heptapeptide (a chain of 7 amino acids) developed at the Institute of Molecular Genetics of the Russian Academy of Sciences in the 1990s under Nikolai F. Myasoedov. Selank itself is the product of extending the endogenous tetrapeptide (a chain of 4 amino acids) tuftsin (Thr-Lys-Pro-Arg; amino-acid fragment 289–292 of the IgG heavy chain) with a stabilizing C-terminal Pro-Gly-Pro tail. That extension yields the Thr-Lys-Pro-Arg-Pro-Gly-Pro sequence — a heptapeptide with dramatically improved resistance to aminopeptidase degradation and a substantially longer duration of action than native tuftsin, while preserving its immunomodulatory (adjusting the immune system up or down) and anxiolytic profile.
The "N-Acetyl" modification layers two further stabilizing changes on top of Selank's own stabilization strategy. The N-terminus is capped with an acetyl group (which blocks the free alpha-amine from attack by aminopeptidases), and the C-terminus is converted from the free carboxylic acid to a carboxamide (-NH₂) via amidation. Both modifications are standard medicinal-chemistry strategies used to raise serum and mucosal stability of short peptides; the same strategy was used to produce N-Acetyl Semax (see Adamax) from parent Semax. The net effect on N-Acetyl Selank, extrapolating from analogous systems, is a longer mucosal residence time after intranasal dosing, slower enzymatic clearance, and an extended window of receptor engagement at equivalent molar doses.
Selank itself is registered in Russia, where it is sold without a prescription (Russian product instructions), under the trade name Selank for generalized anxiety disorder (GAD), adaptation disorders, and neurasthenia. It has not been approved by the FDA, EMA, MHRA, TGA, or any other non-Russian regulator. The N-acetyl amide analog — the molecule on this page — has no regulatory approval anywhere in the world. It is a research-chemical enhancement of the Russian-approved parent and is sold exclusively through research-peptide channels.
For the rest of this page, claims specific to Selank (the Russian-approved parent) are labeled as such; claims specific to N-Acetyl Selank (the stabilized analog) are labeled separately. Conflating the two is a common error in community literature.
Mechanism of Action
Selank's pharmacology is multimodal. The N-acetyl amide modification does not change the fundamental mechanism — it simply extends the duration over which the same mechanisms act. The following describe the mechanism of the active pharmacophore, which is shared between Selank and N-Acetyl Selank:
- GABAergic (related to GABA signaling) allosteric modulation — Selank changes the binding of tritiated GABA to rat brain membranes (V'Yunova 2014) and significantly alters the expression of GABAergic-system genes in the frontal cortex after intranasal dosing (Volkova 2016, Front Pharmacol 7:31). Kozlovskaya 2003 compared Selank with ten tuftsin-family peptides on the behaviour of rats and mice under emotional stress. The model the field works with — Selank as an indirect modulator of GABAA signalling rather than a direct ligand at the benzodiazepine site — is an inference from the gene-expression work above, not a finding of a binding study.
- Serotonin metabolism modulation — Semenova and colleagues (2009) reported Selank-induced changes in brain serotonin metabolism in rats pretreated with para-chlorophenylalanine (PCPA), consistent with a serotonin-pathway contribution to the anxiolytic / antidepressant signal beyond pure GABAergic modulation.
- BDNF upregulation in hippocampus — Intranasal Selank elevates BDNF (brain-derived neurotrophic factor) expression in rat hippocampus (Inozemtseva et al., Dokl Biol Sci 2008). BDNF is a central mediator of adult hippocampal neurogenesis, synaptic plasticity, and cognitive resilience to chronic stress; this limb of Selank's mechanism distinguishes it from classical anxiolytics and provides a plausible nootropic / memory-supportive substrate.
- Enkephalinase inhibition — Selank (and its close relative Semax) inhibits enkephalin-degrading enzymes from human serum (Kost 2001). By extending the half-life of endogenous enkephalins, Selank enhances basal opioidergic tone without engaging mu-opioid agonism itself — a mechanism that may contribute to mood stabilization and to its favorable dependence / tolerance profile.
- Immune / interferon induction — Tuftsin is a natural macrophage-activating peptide; Selank retains part of that profile. Uchakina and colleagues (2008) and Ershov and colleagues (PMID 19882898; 2009) documented antiviral activity of Selank against influenza A (H3N2) in vitro and in vivo, associated with induction of interferon-alpha gene expression. Later work extended the antiviral profile to herpes simplex and cytomegalovirus in culture systems.
- Inflammation-related gene expression — Kolomin and colleagues (2014) followed Selank-induced changes in four inflammation-related genes (C3, Casp1, Il2rg, Xcr1) in mouse spleen after a single injection, suggesting a peripheral immunomodulatory pathway.
- Enhanced pharmacokinetics via acetyl/amide capping — Specific to N-Acetyl Selank: the modifications slow aminopeptidase and carboxypeptidase cleavage of the terminal residues, the rate-limiting enzymatic clearance steps for native Selank. No study has measured how long the capped analog lasts in anyone.
- HPA-axis context — Parent Selank lacks direct HPA-axis activation despite its anti-stress framing — a distinguishing feature from endogenous CRH / ACTH physiology. Its anxiolytic and stress-adaptive signature is built on GABAergic / serotonergic (related to serotonin signaling) / BDNF modulation rather than cortisol suppression or glucocorticoid-receptor engagement.
- Species cross-reactivity — The Russian research program largely characterized Selank in rat and mouse models with intranasal and intraperitoneal administration. Translation to human pharmacology assumes conservation of the GABAA-allosteric and BDNF-upregulation mechanisms across mammalian species, which is a reasonable but not formally verified assumption.
- Nasal-to-brain delivery advantage — Intranasal administration bypasses first-pass hepatic metabolism and delivers a fraction of the dose along olfactory-nerve and trigeminal-nerve routes directly into the CNS, avoiding BBB-related pharmacokinetic losses that would otherwise limit a hydrophilic peptide. This is the standard delivery route for both parent Selank (Russian nasal spray) and the stabilized analog.
What the Research Shows
All interpretable efficacy data comes from the parent Selank molecule. The N-acetyl amide analog has no published study of its own, preclinical or clinical (PubMed, searched October 11, 2026).
- Generalized anxiety disorder (Zozulia 2008, PMID 18454096) — The published pivotal clinical study by Zozulia, Neznamov, Siuniakov and colleagues evaluated intranasal Selank in patients with GAD and neurasthenia. Selank showed anxiolytic efficacy comparable to medazepam (a benzodiazepine) without the sedative or amnestic profile of the comparator, and without the typical benzodiazepine dependence / tolerance signature. This study forms the pharmacoregulatory basis for the parent compound's Russian indication.
- Selank vs diazepam (preclinical synergy) — Kasian et al. (2017) demonstrated that Selank enhances the anxiolytic effect of diazepam in an unpredictable-chronic-mild-stress rat model at a sub-threshold diazepam dose, supporting the allosteric GABAA-modulator interpretation of its mechanism.
- Immune / antiviral signal — Ershov et al. (PMID 19882898) demonstrated antiviral activity of Selank against influenza A/Aichi/2/68 (H3N2) in vitro and in vivo. Selank induced interferon-alpha gene expression without altering IL-4, IL-10, or TNF-alpha. Field reports from Russian influenza prophylaxis programs describe intranasal Selank administration during seasonal influenza outbreaks.
- GABAergic gene-expression signature (Volkova 2016) — Published in Frontiers in Pharmacology (Front Pharmacol 7:31), this study demonstrated significant changes in the expression of genes involved in GABAergic neurotransmission in rat frontal cortex after Selank administration. This is the cleanest molecular-level evidence for the "allosteric GABAA" mechanism claim.
- BDNF upregulation in hippocampus (Inozemtseva 2008) — Intranasal Selank elevated hippocampal BDNF expression in rats, providing the preclinical substrate for claimed nootropic effects.
- Enkephalinase inhibition (Kost 2001) — Semax and Selank both inhibit enkephalin-degrading enzymes in human serum, proposed as a shared mechanism behind their mood-stabilizing and anti-stress effects.
- Behavioral / active-avoidance effects (Kozlovskii & Danchev 2002) — Selank produces optimizing effects on active-avoidance conditioning in rats, an effect pattern consistent with its clinical use in anxiety-mediated cognitive impairment.
- N-Acetyl modification rationale — Rationale inferred from medicinal-chemistry literature on terminal capping of small peptides (reduced aminopeptidase / carboxypeptidase susceptibility) and from analogy to the N-Acetyl Semax stabilization program. Direct pharmacokinetic data on N-Acetyl Selank specifically is limited and unpublished in peer-reviewed literature.
The clinical trial evidence for Selank is (a) Russian-language literature with limited accessibility in Western databases; (b) concentrated in a relatively small group of institutions affiliated with the peptide's developers; and (c) does not extend to the N-acetyl amide analog sold as "N-Acetyl Selank." No controlled human data on the stabilized analog has been published. All mechanistic data shown here for the N-acetyl form is an extrapolation from parent Selank pharmacology plus the general medicinal-chemistry principle of terminal capping. No published study tests the marketing claims of “enhanced” potency.
Human Data
- Zozulia 2008 (PMID 18454096) — Russian-language clinical study of intranasal Selank in generalized anxiety disorder and neurasthenia. Selank showed anxiolytic efficacy comparable to medazepam without sedative, amnestic, or dependence profile. Published in Zhurnal Nevrologii i Psikhiatrii.
- Ershov 2009 (PMID 19882898) — Selank antiviral activity against influenza A/Aichi/2/68 (H3N2) in cell culture and in vivo mouse infection model, with induction of interferon-alpha gene expression.
- Volkova 2016 (PMID 26924987; Front Pharmacol 7:31) — Selank-induced changes in GABAergic-system gene expression in rat frontal cortex; mechanistic support for allosteric GABAA modulator interpretation.
- Inozemtseva 2008 (Dokl Biol Sci 421:241-243) — Intranasal Selank regulates BDNF expression in rat hippocampus.
- Kost 2001 (Bioorg Khim 27:180-183) — Semax and Selank inhibit enkephalin-degrading enzymes from human serum.
- Kasian 2017 — Selank enhances the anxiolytic effect of diazepam in a UCMS rat anxiety model (PMC5322660).
- Kozlovskaya 2003 — Selank and short tuftsin-family peptides in the regulation of adaptive behavior in stress; mechanistic behavioral pharmacology review.
- Uchakina 2008 — Selank-induced cytokine shifts and interferon induction in human leukocyte cultures; immunomodulatory signature extended beyond antiviral context.
- Kolomin 2014 — Temporary dynamics of inflammation-related gene expression under Selank action in mouse spleen.
- Semenova 2009 — Comparison of Selank and tuftsin effects on brain serotonin metabolism in PCPA-pretreated rats.
There are no published human clinical trials specifically of N-Acetyl Selank (the stabilized analog). All positive human data belongs to the parent compound Selank.
Reconstitution & Storage
No label or guideline gives a strength, storage condition or shelf life for N-Acetyl Selank; it is sold as a research chemical. The table is arithmetic only: what a vial of a given size holds once dissolved. It is not a recommendation.
| Vial Size | Diluent | Resulting Concentration |
|---|---|---|
| 5 mg | 2 mL | 2.5 mg/mL (2,500 mcg/mL) |
| 5 mg | 5 mL | 1.0 mg/mL (1,000 mcg/mL) |
| 10 mg | 2 mL | 5.0 mg/mL (5,000 mcg/mL) |
Side Effects & Risks
- What the parent's label lists — An unpleasant taste when the drops run from the nose into the throat, and allergic reactions, including delayed ones; the preservative, methylparaben, can also cause them (Russian product instructions).
- Dependence — The parent's label says it causes no drug dependence or habituation, and no effect on driving (Russian product instructions).
- Pregnancy, breastfeeding, under 18 — Ruled out by the parent's label, because no studies were done (Russian product instructions).
- Interferon — In mice, Selank raised interferon-alpha gene expression in an influenza model (Ershov et al., 2009). What that means for a person has not been studied.
- What is in a vial — N-Acetyl Selank is sold as a research chemical; no analysis of such products appears in the documents read for this page.
- Long-term safety — No study of the capped version, of any duration, has been published (PubMed, searched October 4, 2026).
Bloodwork & Monitoring
No trial, label or guideline sets monitoring for N-Acetyl Selank, and no study of it has been published. The parent’s Russian instructions list no laboratory tests (Russian product instructions), and the 2008 trial rated patients on the Hamilton, Zung and CGI scales and measured enkephalin activity in their serum (Zozulia et al., 2008).
Commonly Stacked With
No published study has combined N-Acetyl Selank with anything. FDA’s reviewers found a US website selling a premixed 50:50 Semax and Selank spray and injection — the parent compounds, not this analog (FDA Semax briefing, 2026).
Legal Status
Parent Selank is approved in Russia and sold there without a prescription (Russian product instructions), as Selank 0.15% nasal drops / spray, for generalized anxiety disorder, neurasthenia, and adaptation disorders. It is not approved by the U.S. FDA, European Medicines Agency, U.K. MHRA, Australian TGA, or Health Canada.
N-Acetyl Selank (the stabilized analog on this page) is not approved by any regulatory agency anywhere in the world. It is distributed as a research peptide labeled "not for human use" and has no clinical-trial pedigree of its own.
Neither N-Acetyl Selank nor its parent, Selank, is specifically named on the WADA Prohibited List. No Selank-family peptide has been flagged as a routinely tested substance. WADA’s S0 clause (non-approved substances) prohibits at all times any pharmacological substance that no other section covers and that no government health authority has approved for human therapeutic use (WADA Prohibited List 2026). Selank itself is registered as a medicine in Russia, so S0 does not apply to it; N-Acetyl Selank has no such approval, so S0 prohibits it at all times.
Neither Selank nor N-Acetyl Selank is on the FDA Category 2 Bulk Drug Substances list, and neither was among the 12 peptides FDA removed from that list in April 2026 (FDA 503A categories list, April 22, 2026). Given the lack of a U.S. regulatory sponsor, Selank-family compounds are unlikely to enter FDA-compoundable status in the foreseeable U.S. regulatory horizon.
N-Acetyl Selank is available through research-peptide suppliers labeled for laboratory research purposes only. It is not dispensed through U.S. or EU regulated pharmacies. Parent Selank is sold as a finished nasal spray pharmaceutical in Russia and in some other CIS markets; personal-use import into the U.S. exists in a legal gray area.
Access quality through unregulated channels varies significantly. Kalios does not sell compounds or endorse their use.
N-Acetyl Selank was not among the 12 peptides FDA removed from Category 2 in April 2026 (FDA 503A categories list, April 22, 2026). Barring a formal U.S. NDA sponsor, it will remain a research-only compound in U.S. regulatory terms.
Access as of April 2026. Actual availability and pricing vary by source and jurisdiction. Kalios does not sell compounds.
Next Steps
References
- Zozulia AA, Neznamov GG, Siuniakov TS, Kost NV, Gabaeva MV, Sokolov OIu, Serebriakova EV, Siranchieva OA, Andriushenko AV, Telesheva ES, Siuniakov SA, Smulevich AB, Miasoedov NF, Seredenin SB. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):38-48. PMID: 18454096.
- Volkova A, Shadrina M, Kolomin T, Andreeva L, Limborska S, Myasoedov N, Slominsky P. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 2016 Feb 18;7:31. PMID: 26924987.
- Ershov FI, Uchakin PN, Uchakina ON, Mezentseva MV, Alekseeva LA, Miasoedov NF. Antiviral activity of immunomodulator Selank in experimental influenza infection. Vopr Virusol. 2009;54(5):19-24. PMID: 19882898.
- Inozemtseva LS, Karpenko EA, Dolotov OV, Levitskaya NG, Kamensky AA, Andreeva LA, Grivennikov IA. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Dokl Biol Sci. 2008;421:241-243. PMID: 18841804.
- Kost NV, Sokolov OYu, Gabaeva MV, Grivennikov IA, Andreeva LA, Miasoedov NF, Zozulia AA. Semax and selank inhibit the enkephalin-degrading enzymes from human serum. Bioorg Khim. 2001;27(3):180-183. PMID: 11443939.
- Kasian A, Kolomin T, Andreeva L, et al. Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats. Behav Neurol. 2017;2017:5091027. PMC5322660.
- Kolomin T, Shadrina M, Slominsky P, Limborska S, Myasoedov N. A new generation of drugs: synthetic peptides based on natural regulatory peptides. Neurosci Med. 2013;4(4):223-252. DOI: 10.4236/nm.2013.44035.
- Kozlovskaya MM, Kozlovskii II, Val'dman EA, Seredenin SB. Selank and short peptides of the tuftsin family in the regulation of adaptive behavior in stress. Neurosci Behav Physiol. 2003;33(9):853-860. PMID: 14969422.
- Seredenin SB, Kozlovskaia MM, Blednov IuA, Kozlovskii II, Semenova TP, Czabak-Garbacz R. The anxiolytic action of an analog of the endogenous peptide tuftsin on inbred mice with different phenotypes of the emotional stress reaction. Zh Vyssh Nerv Deiat Im I P Pavlova. 1998;48(1):153-160. PMID: 9583175.
- Kozlovskii II, Danchev ND. The optimizing action of the synthetic peptide selank on an active avoidance reflex in rats. Zh Vyssh Nerv Deiat Im I P Pavlova. 2002;52(5):579-584. PMID: 14552529.
- Semenova TP, Kozlovskii II, Zakharova NM, Kozlovskaia MM. Comparison of the effects of selank and tuftsin on the metabolism of serotonin in the brain of rats pretreated with PCPA. Eksp Klin Farmakol. 2009;72(4):6-8. PMID: 19803361.
- Kolomin T, Morozova M, Volkova A, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N. The temporary dynamics of inflammation-related genes expression under tuftsin analog Selank action. Mol Immunol. 2014;58(1):50-55. PMID: 24291245.
- Uchakina ON, Uchakin PN, Miasoedov NF, Andreeva LA. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(5):71-75. PMID: 18577961.
- Andreeva LA, Nagaev IY, Mezentseva MV, Shapoval IM, Podchernyaeva RY, Shcherbenko VE, Potapova LA, Rusakova EV, Miasoedov NF. Antiviral properties of structural fragments of the peptide Selank. Dokl Biol Sci. 2010;431:86-88. PMID: 20506839.
- FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
- World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.
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Tested together in people
None published · Read the receipt →
Checked 18 Oct 2026